Tag Archives: bacteria

Artificial bacteria-killing cells could win the war against drug resistance

Research at the University of California, Davis, has resulted in artificial cells that cannot grow or divide but will unleash a can of whoop-ass on any bacteria they encounter.

The artificial cells mimic some of the properties of living cells but don’t grow and divide.
Image credits Cheemeng Tan / UC Davis.

Although researchers have successfully created artificial cells in the past, they remained stable only in certain conditions. The key limitation was that these cells could only survive in nutrient-rich environments, as they lacked the capacity to feed themselves.

The advancement this present paper reports on is that the team’s “lego block” artificial cells can survive and work in a wide variety of conditions with limited resources. This greater self-sufficiency was achieved by the team’s efforts in refining the cells’ membranes, cytosol (the ‘soup’ inside cells), and their genetic material.

Teeny-weenie death machinie

“We engineered artificial cells from the bottom-up — like Lego blocks — to destroy bacteria,” said Assistant Professor Cheemeng Tan, who led the work.

“We demonstrated that artificial cells can sense, react and interact with bacteria, as well as function as systems that both detect and kill bacteria with little dependence on their environment.”

The cells are built from liposomes — bubbles with a cell-like lipid membrane — and purified cellular components including proteins, DNA, and assorted metabolites. They have all the fundamental components of live cells, but they’re short-lived and cannot divide, so they can’t make more of themselves.

The cells were forged with a purpose, however — to beat up E. coli bacteria. By tweaking their genetic material, the team designed these cells to pick up on and react to a unique chemical signature given off by E. coli. Laboratory tests showed that once these artificial cells pick up on the scent, they will attack and destroy all E. coli in a culture.

As the cells are much more robust and self-sufficient than previous ‘models’, they can be employed even in less-than-ideal or changing conditions. This enables them to have a much broader scope of potential applications compared to any other artificial cells currently at our disposal.

The team has high hopes for their spawn. The researchers envision using these cells in an antibacterial role, injecting them into patients suffering from infections resistant to conventional treatments. Alternatively, they might be used for targeted delivery of drugs at specific locations and times, or as biosensors.

The paper “Minimizing Context Dependency of Gene Networks Using Artificial Cells” has been published in the journal Applied Materials and Interfaces.

Brown bear.

Brown bear saliva kills a bacteria that current antibiotics are unable to treat

An international research team reports that the saliva of a Siberian brown bear (Ursus arctos collaris) subspecies can kill Staphylococcus aureus bacteria, a strain that is rapidly becoming resistant to all current antibiotics.

Brown bear.

Image credits Oksanna Briere.

One subspecies of the Siberian brown bear can kill S.aureus with its bare saliva, a new paper reports. The animal’s range includes Mongolia, Siberia, and parts of northern China. While generally vegetarian, the bears also dine on caribou, elk, and fish. This wide menu has a profound impact on the subspecies’ microbiome, the team writes — including its surprising disinfectant ability.

‘Drool over this, please’

The discovery comes as part of a larger project aiming to study the microbiome of several wild animals. The project’s goal is to find naturally-occurring chemicals which can kill bacteria that also infect humans, especially the strains that are becoming or have become resistant to antibiotic treatments.

The team captured several specimens of the bear subspecies in the taiga — the forested parts of Siberia — and harvested saliva swabs for analysis. Using “state of the art screening techniques,” the team was able to identify the chemical make-up and microbiota of the samples.

One bacteria swimming its merry way in that saliva is Bacillus pumilus, a strain that secretes an antibiotic compound known as amicoumacin A. The team believes the bears obtain this bacterium when they munch on certain types of vegetation.

After finding B.pumilus in the saliva samples, the team looked to see how it interacts with other antibiotic-resistant bacteria such as S.aureus — which is associated with skin infections in humans. That’s how they discovered that the strain can effectively deal with the staphylococcus.

The findings could go a long way in hospitals and other healthcare facilities, which are struggling to remove the deadly bacteria. A naturally-occurring chemical that can help us fight staph would be quite valuable.

The team plans to continue the project in hopes of finding even more new compounds that can help us keep bacteria at bay.

The paper “Ultrahigh-throughput functional profiling of microbiota communities” has been published in the journal PNAS.


Why you shouldn’t pop your pimples — Really, you shouldn’t

Credit: Pixabay.

Popping pimples can be very tempting, but this is considered a bad idea by most dermatologists. Picking at your blemishes can spread infection and ultimately worsen your acne. It can also permanently scar your face. If you do insist on getting rid of the pimples, there are more hygienic and safe methods you should use — never do it with your bare hands, that’s for sure.

How pimples form

It helps the discussion if we first learn what causes blemishes.  It all starts in the hair follicles which contain the oil-secreting sebaceous glands. These glands are found the most on the face and scalp compared to other parts of the body, and there’s no coincidence why these areas are the most prone to pimples.

The glands’ function is to secrete oil to lubricate the hair, but when hair or skin dies the pores the oil oozes through are blocked. This creates an excess of oil in the pores which are forced by physics to expand under the skin in the shape of a water balloon. By this time, the skin looks red, puffy and infected.

When you squeeze a pimple, there’s a high risk of forcing debris of bacteria and dead skin deeper straight to the follicle. The follicle wall might rupture then and spill infected material into the dermis, which is the innermost layer of the skin. Even if you pull out a lot of that nasty goo, chances are infected material tunneled the dermis from below because of the pressure you exerted.

Popping pimples can lead to:

  • Scarring. This is quite rare and happens when you pick a pimple so deeply so that you would get a hole. It can still happen though when some people get carried overboard.
  • Scabs. A big white head pimple can ruin your morning, especially if a meeting is due but living with it may be better than the alternative: a nasty, crusty scab. This happens because the skin thickens or darkens to protect itself from injury. Unfortunately, brown spots or hyperpigmentation is harder to clear up than a pimple itself and can take months to get rid of.
  • Infection. In some cases, medical attention may be required.
  • Pain. Especially the big ones — those hurt like hell.
  • New pimples. The good from a squeezed pimple can block other pores and lead to the formation of new pimples.

A hands-off approach when it comes to your skin may be for the best, even though it might seem socially awkward not to.

How to pop a pimple the right way

Whiteheads will come away by themselves in about a week, which might seem like an eternity to a teenager. If you really insist, there are some safe methods you can use to get rid of some pimples.

Use two cotton swabs instead of your fingers, or better yet a sterilized needle. Wait for the pimple to come to a head, then squeeze with the cotton swabs. Stop squeezing when you see blood and then spot-treat the pimple by applying a tiny bit of hydrocortisone. Make sure you apply it only on the zit.

Before attempting anything, it’s important you thoroughly wash your hands and rub alcohol on your fingers to sterilize them. Always apply pressure gently so you don’t push debris down the follicle.

If you have a nuclear meltdown on your face, then you could visit a dermatologist. The doctor will use special tools like a cortisone shot or even lasers to extract your whiteheads and blackheads or drain a cyst.

If it’s a blind pimple — big red bumps under the skin– then there’s nothing you can do. Attempting to pop it will only make it worse as you can get the skin injured. Wait for it.

Credit: Pixnio.

Bacterial superbugs have become up to 10 times more tolerant to alcohol-based hand sanitizers

Credit: Pixnio.

Credit: Pixnio.

Many hospitals around the world have installed hand sanitizers for staff, visitors, and patients to use. However, the bacteria was quick to react. A new study found that superbugs found in Australian hospitals have become up to ten times more tolerant to alcohol exposure, the key ingredient in hand sanitizers.

These bacteria hold their liquor

After hospitals across Australia started massively adopting alcohol-based hand sanitizers in the early 2000s, the rate of infections dropped, signaling that the introduction had a positive effect. Other types of infections, however, weren’t reduced. In fact, the incidence of some infections — enterococcal infections, in particular, which affect the digestive tract, bladder, and heart — actually went up. And this wasn’t happening just in Australia, but around the world.

Enterococci infections are the leading cause of sepsis — a life-threatening condition in which the body is fighting a severe infection that has spread via the bloodstream — and are responsible for around 10% of bacterial infections acquired from hospitals.

Researchers at the University of Melbourne’s Doherty Institute for Infection and Immunity compared 139 types of bacterial strains collected between 1997 and 2015. The cultured bacteria collected after 2009 were up to 10 times more tolerant to alcohol than pre-2004 bacteria — the year the local government pushed the use of hand sanitizers in hospitals.

These bacteria aren’t resistant to alcohol, not yet at least. However, they’ve built up a huge tolerance. When the researchers incrementally raised the concentration of alcohol to which each type of bacteria was exposed, the tolerant-variety started dying at around 70% alcohol mixture, whereas most hand sanitizers carry 60% alcohol.

One of the greatest challenges in modern medicine is the growing problem of antibiotic resistance, which occurs when an antibiotic is no longer effective at controlling or killing bacterial growth. Bacteria which are ‘resistant’ can multiply in the presence of various therapeutic levels of an antibiotic. Sometimes, increasing the dose of an antibiotic can help tackle a more severe infection but in some instances — and these are becoming more and more frequent — no dose seems to control the bacterial growth. Each year, 25,000 patients from the EU and 63,000 patients from the USA die because of hospital-acquired bacterial infections which are resistant to multidrug-action.

What’s worrisome about these latest findings is that many of the alcohol-tolerant bacteria are also resistant to multiple antibiotics. For instance, half of such bacterial strains don’t respond to vancomycin, a very potent antibiotic which is typically used as a last line of defense when treating infections.

Writing in Science Translational Medicinethe researchers recommend that hospitals should adhere to stricter sanitizing procedures. Feeling confident that alcohol sanitizers destroy most bacteria, medical staff might feel overly confident that they’re hands are sanitized, not bothering to use soap and water afterward. However, the simple act of rubbing bacteria off the skin is still one of the most effective methods for controlling bacterial infections. This latest study should serve as a reminder.

In the future, research will have to establish which is a safe alcohol-threshold for modern sanitizers to use. It might even be possible that some bacteria will become resistant to alcohol.



Bacteria lip print.

Bacteria species, too, can become extinct — and they do so quite often

Evolution is ruthless even with its tiniest creations.

Bacteria lip print.

Image credits Bnummer / Wikimedia.

New research led by researchers from the University of British Columbia (UBC) reports that bacteria also die off — and they do so at substantial rates. The findings go against the grain of the widely-held notion that bacterial species, owing to their very large populations, rarely go extinct.

To kill a M. ocking bacteria

Bacteria are, by far, one of the most prolific and successful bits of life that evolution spawned on our planet. They’re incredibly hardy, very good at drawing energy from their environments, and they reproduce with a vengeance. These tiny critters are so resilient and numerous, in fact, that most scientists took it as a given that bacteria species very rarely go extinct. However, new research suggests that this isn’t the case.

The team sequenced DNA information from 448,112 different bacterial species and drew on 60 previous environmental studies to create the most comprehensive bacteria evolutionary tree, which includes the majority of bacterial species over the past billion years. To get an idea of bacteria’s evolutionary history, they drew on the traces that speciation (differentiation of new species through evolution) leaves in the genetic makeup of these bacterial lineages.

The team estimates that there are around 1.4 to 1.9 different bacterial phyla (lineages) gracing our planet today. They were also able to estimate how that number varied over time: they report that anywhere between 45,000 to 95,000 phyla became extinct over the last million years.

“Bacteria rarely fossilize, so we know very little about how the microbial landscape has evolved over time,” says Stilianos Louca, lead researcher of the study. “Sequencing and math helped us fill in the bacterial family tree, map how they’ve diversified over time, and uncover their extinctions.”

It’s an impressive number. But, despite these relatively high extinction rates (which the team notes were quite steady over time), bacteria have kept diversifying exponentially throughout history. As a group, they also managed to weather planet-wide mass extinction events — those abrupt events that periodically cull plant and animal species — with very few losses. All in all, while the current number of bacterial lineages today is definitely impressive, “it’s only a tiny snapshot of the diversity that evolution has generated over Earth’s history,” Louca adds.

“This study wouldn’t have been possible 10 years ago,” says Michael Doebeli, senior author of the paper and a UBC mathematician and zoologist. “Today’s availability of massive sequencing data and powerful computational resources allowed us to perform the complex mathematical analysis.”

Next, Louca says he and his team plan to determine how the physiological properties of bacteria evolved over time. A particular point of interest for them is determining whether their ecological diversity has increased in tow with their taxonomic diversity — i.e. if they spread to new types of environments and roles in those environments as the total number of species increased. If so, this would suggest that even organisms as ancient and simple as bacteria can still find new roles in nature.

The paper “Bacterial diversification through geological time” has been published in the journal Nature ecology and evolution.

Salmonela phage.

New U.S. Center to research how viruses can help us overcome drug resistance

In a bid to fight drug-resistant infections, one group of U.S. researchers is trying to include bacteria-munching viruses on our list of available treatments.

Salmonela phage.

Salmonela phage PA13076.
Image credits microbiologybytes / Flickr.

Amid the rise of drug-resistant bacteria and the string of outbreaks in recent years — most notably the Ebola virus in Africa, Zika in South America, and the Nipah virus outbreak in India — it may feel like everything microscopic is out to get us. But fret not: nature doesn’t discriminate; there’s something to infect everything under the sun.

One group of researchers from the University of California, San Diego (UCSD) plans to cash in on this by using bacteria-hunting viruses — phages — to knock out drug-resistant infections, the university reported recently.

The enemy of my enemy

The initiative stems from the efforts of UCSD researchers who 2 years ago used phages to save a colleague’s life. In 2015, UCSD psychologist Tom Patterson was hospitalized after a drug-resistant strain of the bacterium Acinetobacter baumannii invaded his pancreas during a vacation in Egypt. Antibiotic treatment failed and Patterson fell into a coma. His wife, UCSD epidemiologist Steffanie Strathdee, launched an international effort to find the right phage to cure him — and, using strains donated by biotech AmpliPhi Biosciences, Texas A&M University, and the U.S. Navy, she did.

Building on that success, the team wants to expand the use of phage therapy in the U.S. Phages are naturally-occurring strains of viruses that live in all sorts of environments and prey on bacteria. They’re really, really good at killing bacteria, much more so than any antibiotics we’ve developed. They’re also single-minded in their purpose, and phage therapy has little to no side effects. However, it’s not flawless: each phage targets only a specific strain of bacteria — so actually using them as a treatment means sifting through millions of strains to find the one that works.

Patterson received some of the phages intravenously — considered to be a risky option, as toxins produced by bacteria used to grow the phages could linger in the mixture. The team’s success in Petterson’s case helped cement their belief that phage therapy can bring an important contribution to modern medicine.

Past pushes towards phage therapy across the globe, however, have fared quite poorly, and the approach isn’t widely considered as a viable treatment path. Phages’ ability to attack a single strain at a time is what gave researchers the most trouble and, for many, signaled that it’s simply not worth pursuing. Previous phage clinical testing, such as an EU-sponsored trial known as PhagoBurn, haven’t been very successful — in part because it focused on treating burn wounds, which typically involve several strains of bacteria. Still, there were some encouraging results regarding phage therapy, mostly from centers in Georgia and Poland. In the context of rising antibiotic-resistance, a few U.S. companies and research centers have also started reconsidering phage therapy.

Since Patterson’s recovery, the UCSD team has successfully cleared infections in five more people with phage cocktails under a U.S. Food and Drug Administration (FDA) process designed for emergencies where no approved treatments are available. However, these are anecdotal evidence, and any phage therapy that has the slightest hope of getting FDA approval needs reliable evidence that it’s safe and effective. That kind of evidence can only be brought to bear following structured clinical trials.

The team hopes their new center will help provide such evidence. A first in North America, the center will initially consist of 16 UCSD researchers and physicians. It will launch with a 3-year, $1.2 million grant from UCSD. Christened the Center for Innovative Phage Applications and Therapeutics (IPATH), it won’t manufacture any phage treatments itself but will collaborate with academia and companies on clinical trials. Initially, IPATH will focus on treating patients suffering from chronic drug-resistant infections related to organ transplants, implanted devices (e.g. pacemakers or joints), and cystic fibrosis.

The trials to be carried out at IPATH will also draw wisdom from past failures with phage therapy. Most notably, it will focus on patients infected with a single (and known) bacterial strain. While it may be difficult to tease out the effects of phage therapy alone (as these patients are undergoing antibiotic treatment, and discontinuing them isn’t an option) the team expects phage therapy to eventually be used in tandem with antibiotics.

One of the main hurdles IPATH collaborators will have to overcome is that current drug approval systems just aren’t suited to accommodate phage therapy. They’re meant to estimate single compounds that can affect patients more or less equally — phage therapy, on the other hand, requires mixes of viruses that need to be tailored for each individual. One potential workaround to this issue would be to get approval for an entire library of phages from which doctors can later create custom treatments. In the meantime, the UCSD team plans to keep securing phages for individual cases under FDA’s emergency pathway, Strathdee says.

Kitchen towels are packed with bacteria, but should you really be worried?

Your kitchen towels may be teeming with bacteria, some of which may cause food poisoning.

Credit: Pixabay.

These were the findings recently reported by researchers at the University of Mauritius, who collected 100 kitchen towels after a month of regular use and washing. The members of the household from where the towels had been collected were interviewed about their living conditions.

Researchers found that 49 of these samples were infected with bacteria, including Escherichia coli (E. coli), Enterococcus, Staphylococcus aureus (S. aureus).

E. coli is a normal bacteria found in the intestine and is released in large numbers in human feces while S. aureus is a bacteria found in the respiratory tract. Both can cause food poisoning, whose symptoms include nausea, explosive vomiting for up to 24 hours, abdominal cramps/pain, headache, weakness, diarrhea and usually a subnormal body temperature.

The most bacteria were found in towels collected from meat-eating families or those with many children. Towels that were used for a variety of tasks — such as wiping utensils, dryings hands, cleaning surfaces, and holding hot objects — had more bacteria than those used solely for one purpose. Damp towels were also more infected than dry ones, the authors of the study reported at the American Society for Microbiology meeting held this weekend in Atlanta, Georgia.

A study published in 2014 by Drexel University researchers came to similar conclusions, finding E. coli on almost 26 percent of towels. Another food-handling study published in 2015 found cloth towels were the most contaminated.

In order to avoid cross-contamination in the kitchen, people are advised to properly wash their hands. You should avoid using towels in place of hand-washing because they can easily become contaminated with harmful germs from raw meat and poultry juices.

“Humid towels and multipurpose usage of kitchen towels should be discouraged. Bigger families with children and elderly members should be especially vigilant to hygiene in the kitchen,” said lead author Susheela Biranjia-Hurdoyal in a statement.

Researchers have figured out how some soil bacteria turn antibiotic drugs into food. Credit: Michael Worful.

Some bacteria eat antibiotics — and this might actually be a good thing

Researchers have figured out how some soil bacteria turn antibiotic drugs into food. Credit: Michael Worful.

Researchers have figured out how some soil bacteria turn antibiotic drugs into food. Credit: Michael Worful.

You might have heard all about how many bacterial strains are becoming resistant to even our strongest antibiotics. The most immediate (and frightening) consequence is that humanity risks reverting to a dark age of medicine where unstoppable infectious diseases spread like wildfire. What’s truly mindboggling is that not only have some strains become resistant to antibiotics, they’ve learned to embrace them, consuming them for food.

Researchers at the Washington University School of Medicine in St. Louis have investigated what freaky biology allows bacteria to ingest as food what would normally be poison for them. Writing in the journal Nature Chemical Biologythe authors say that three distinct set of genes become active in trials when the bacteria ate penicillin but stayed inactive while the bacteria ate sugar.

The researchers worked with four distinct species of soil bacteria. These species likely gained antibiotic resistance due to the unregulated dumping of antibiotic-laden waste into local waterways, which also ends up in the soil. Because bacteria easily share genetic material, the antibiotic-resistant genes quickly spread through the community.

Each of the three genes identified by the researchers corresponds to one of three steps the bacteria take in order to consume antibiotics as food. First, the bacteria neutralize the dangerous part of the antibiotic which is toxic to them. With the toxin disarmed, the bacteria are then free to consume the matter which is essentially just like any other carbon-based food at this point.

“Ten years ago we stumbled onto the fact that bacteria can eat antibiotics, and everyone was shocked by it,” said senior author Gautam Dantas in a statement. “But now it’s beginning to make sense. It’s just carbon, and wherever there’s carbon, somebody will figure out how to eat it. Now that we understand how these bacteria do it, we can start thinking of ways to use this ability to get rid of antibiotics where they are causing harm.”

Antibiotic resistance is no joke. Whenever bacteria survive an antibiotic onslaught, it can acquire resistant through mutation of the genetic material or by ‘borrowing’ pieces of DNA that code for the resistance to antibiotics from other bacteria, like those from livestock. Moreover, the DNA that codes the resistance is grouped in an easily transferable package which enables the germs to become resistant to many antimicrobial agents.

In a previous long-form article, I wrote:

“Before Alexander Fleming discovered penicillin in 1928, there was no effective treatment for infections such as pneumonia, gonorrhea or rheumatic fever. Fleming’s discovery kicked off a golden age of antimicrobial research with many pharmaceutical companies developing new drugs that would save countless lives. Some doctors in the 1940s would famously prophesize that antibiotics would finally eradicate the infectious diseases that had plagued humankind throughout history. Almost a hundred years later since Fleming made his milestone discovery not only are bacterial infections still common, the misuse and overuse of antibiotics are threatening to undo all of this medical progress.”

According to the CDC, the following bacterial strains have developed the most resistance such that they’ve been listed as urgent hazards:

  • Clostridium difficile. Causes severe diarrhea, especially in older people and those who have serious illnesses.
  • Enterobacteriaceae. These normally live in the digestive tract but can invade other parts of the body, like the urinary tract, and cause infections.
  • Neisseria gonorrhoeae. Causes gonorrhea, a sexually transmitted infection. In 2016, the WHO said gonorrhea might soon become untreatable. 

However, although antibiotic-munching bacteria sound terrifying, the authors of the new study say their adapted abilities could be exploited in our favor. One of the reasons so many bacteria develop resistance in the first place is due to poor waste management. In China and India — the world’s most important producers of pharmaceuticals — it’s common practice for waste leftover from the antibiotic manufacturing process to end up in waterways. So, why not use the antibiotic-resistant bacteria to clean up such dumps? That would be one primary application of the recent findings.

“Of course, the benefits of any such bioremediation program would need to be weighed against the risk of releasing a genetically modified bacterium into the environment and the potential spread of antibiotic resistance/degradation genes to other organisms,” the authors wrote.

“Before starting this project, we already knew that a lot of bacteria in the soil could eat antibiotics, and we all would have been very surprised if it had turned out they were somehow doing this without using antibiotic resistance genes in some way. So I think that it is mostly good news that, while resistance is part of this pathway, we now have the blueprints for how bacteria eat an antibiotic. We actually used this knowledge to design a benign strain of laboratory E. coli to do an even better job eating penicillin,” Terence Crofts, first author of the new paper and a researcher at the University of Washington, told ZME Science.

One major challenge is that the soil bacteria capable of eating antibiotics are difficult to work with and the rate at which they consume the drugs is far too slow to make an impact. The researchers, however, are confident that they can engineer E. coli, which is a well-studied bacteria and a far more tractable species, for this purpose. In experiments, the Washington University researchers showed that they could give E. coli antibiotic-eating abilities, allowing it to thrive on penicillin. The bacteria usually requires sugar to survive, but due to genetic modifications and the presence of a key protein, the E. coli survived on a sugar-free diet of penicillin.

“I think an important take-away from this paper is how we look at antibiotics. We (humans) see antibiotics just as a medicine we get from the clinic, but most of our antibiotics are actually chemicals that are made by or based on compounds that soil bacteria and fungi use to compete against their neighbors. So from the point of view of soil microbes, antibiotics are just another type of carbon-based molecule that while sometimes toxic are fair game for eating if they can be detoxified. When we consider antibiotics as being by and for bacteria, it makes sense that antibiotic resistance and antibiotic degradation/eating are widespread in the soil,” Crofts concluded.

Credit: Pexels.

NYC mice are crawling with antibiotic-resistant bacteria and viruses

Credit: Pexels.

Credit: Pexels.

Rats get all the bad rep in New York City but it’s their smaller, more low-key cousins that could be far more dangerous pests. According to a new study, mice living in the basements of New York City apartments carry some bacteria and viruses that haven’t been seen before. What’s more, some of the bugs are resistant to antibiotics.

Of mice and bugs

Researchers at Columbia University collected feces from more than 400 mice captured over a period of one year in buildings in Manhattan, Brooklyn, Queens, and the Bronx. Most of the mice were caught in or around garbage disposal areas in sub-basements, though five mice were trapped in the food preparation/storage areas of a commercial building, and a single mouse was captured in somebody’s apartment.

The findings were reported on in two separate studies. The first, published in the journal mBio (the journal of the American Society for Microbiology), found that the rodents carried previously unseen viruses, as well as bacteria capable of causing life-threatening illness in humans. When they focused on the bacteria more closely, researchers detected several famous disease-causing pathogens like Shigella, Salmonella, Clostridium difficile, and E. coli. 

The most worrisome part of this study was the fact that some of these bacteria were antibiotic-resistant, similarly to those that have become nearly untreatable in area hospitals.

“From tiny studios to penthouse suites, New York City apartments are continually invaded by house mice,” says lead author Simon H. Williams, BSc, a research scientist at the Center for Infection and Immunity. “Our study raises the possibility that serious infections—including those resistant to antibiotics—may be passed from these mice to humans, although further research is needed to understand how often this happens, if at all.”

Salmonella infections are generally a result of eating food contaminated with animal waste — including mouse feces. In the U.S. alone, there are about 1.4 million reported cases of Salmonella infections annually along with 15,000 hospitalizations and 400 deaths.

The second study, also published in mBio, provides a detailed look at viruses present in the mice droppings. The mice carried 36 viruses, six of which are completely new to science. Fortunately, none of the identified viruses are known to infect humans. On the other hand, researchers identified genetic sequences matching viruses that are known to infect dogs, chicken, and pigs. This suggests that some of these viruses may have crossed over from other species — and if they did once before, they might do it again.

“New Yorkers tend to focus on rats because they are larger and we see them scurrying around in streets or subways; however, from a public health vantage point, mice are more worrisome because they live indoors and are more likely to contaminate our environment, even if we don’t see them,” says senior author W. Ian Lipkin, MD, senior author of both papers, John Snow Professor of Epidemiology, and director of CII.

Despite the numerous disease-carrying pathogens, the mice were generally healthy, signaling they’re carriers that are not affected by the bacteria. It’s unclear at this point how much of a threat these mice pose to people, or whether they’ve caused any human disease. The latter part would be impossible to prove by any research, in any case — the source of a patient’s infection is rarely investigated and they are not usually asked about any contact with mice. The real takeaway, according to Lipkin, is that “these things are everywhere.”

It’s also unclear whether the mice acquired these antibiotic-resistant bacteria from people — for instance, by eating food contaminated with feces from a person who was taking antibiotics — or whether the bacteria developed the resistance to the bacteria after exposure to discarded antibiotics. Despite that the source of the resistance is unknown, what’s certain is that the NYC mice harbored bacteria with 22 different genes that could confer resistance to a number of common classes of antibiotic drugs, including the quinolones, macrolides, and ß-lactams.

“These antibiotic resistance genes are out there in the environment and mice are carrying them everywhere,” Lipkin said. “My concern is that they are a reservoir of antibiotic resistance.”

Overall, the researchers found that more than a third (37%) of the mice carried at least one potentially pathogenic bacterium and almost one quarter (23%) of the mice harbored at least one antimicrobial resistance gene in their fecal bacteria. 

“We used to think of mosquitoes as the source of just an itchy bite, but now we know they carry Zika virus and West Nile virus,” says Lipkin. “We should be thinking of mice in the same way, as potential sources of infection. And that means we should control them as vectors of disease.”

Are hand dryers actually hygienic? New study found they spread fecal bacteria all over your hands

Credit: Wikimedia Commons.

Credit: Wikimedia Commons.

A lot of people cringe at the idea of visiting public restrooms but few have any qualms with hand dryers — after all, they just blow hot air and never come into direct contact with your body. However, you should know that they’re far from harmless. Researchers at the University of Connecticut analyzed the outflow of hand dryers in various public restrooms and found they were dispersing Bacillus subtilis, a bacteria commonly found in human feces, all over the room.

Debris, like dust and skin but also microbes, are constantly being circulated through a public restroom as people move in and out. Especially when a lidless toilet is flushed. Because hand dryers suck the ambient air in the restroom and then spew it out at high velocity, these machines actually expose you to more microbes — at least, that’s what a new study found after growing bacterial colonies collected from either bathroom air or blow dried air.

When the hand dryers were off, only six colonies on average grew per plate. However, with the blow dryers up and running, so were the bacteria: as many as 60 colonies, on average, grew per plate, as reported in the journal Applied and Environmental Microbiology. Overall, 62 types of various bacteria representing 21 species were identified by the researchers, including Staphylococcus aureus, which can sometimes cause serious infections.

The team of researchers investigated airborne bacteria in 36 bathrooms at the University of Connecticut School of Medicine. In every tested bathroom, the researchers discovered a lab-engineered strain of the common soil bacteria Bacillus subtilis called PS533. This strain is never found in nature and exclusively appears in laboratory settings. What happened was bacterial spores likely traveled from labs, either carried by air or people’s movements, to all sorts of other rooms in the research building, including bathrooms. The PS533 strain is totally harmless to humans but its presence in each and every one of the tested environments highlights just how easy it is for bacteria to spread.

The new findings are important for healthcare facilities and other environments where sanitation is king. However, for the most part, the new study shouldn’t worry anyone since our immune system can handle the kind of bacteria that’s blown on our hands and faces. And yes, there are ways to minimize restroom-bacteria exposure. The researchers found that adding high-efficiency particle air (HEPA) filters blocked 75% of the bacteria blown by the hand dryers — but that’s still not perfect. If you want to be extra safe, the best option to dry your freshly cleaned hands is also one of the simplest: use paper towels. Previously, another study found state-of-the-art blow dryers spread 1,300 more virus clumps than paper towels. Unfortunately, paper towels create waste, so perhaps not drying your hands at all might be the best thing to do.

Antibiotic resistance infograph.

The CDC thwarted 220 cases of pathogens with ‘unusual’ antibiotic resistance last year alone

Over 220 instances of germs with ‘unusual’ antibiotic resistance genes were reported to the CDC across the U.S., the CDC’s Vital Signs report states.


Image via Pixabay.

The increasing prevalence of drug-resistant bacteria is, for good reason, one of the most worrying trends in modern medicine. Simply put, we’re developing new treatment options much more slowly than bacteria and their ilk can adapt (read: become immune) to the ones currently at our disposal.

In light of this fact, I’m sure you’ll be comforted to hear that health departments working with CDC’s Antibiotic Resistance (AR) Lab Network throughout the U.S. found more than 220 instances of germs with ‘unusual’ antibiotic resistance genes last year, according to the Vital Signs report. This category includes germs that are impervious to most or all antibiotics we currently possess, are uncommon in one particular geographic area or the U.S. as a whole, or have genetic mechanisms that allow them to spread their resistance to other germs.

To kill a mockinggerm

Antibiotic resistance infograph.

Image credits CDC.

Needless to say, because of the danger they pose to public health, the CDC considers the early detection of these pathogens a top priority. After a threat is identified, the next step in the Centers’ strategy is containment: facilities working with the CDC’s AR Lab try to isolate infected patients as quickly as humanly possible, then initiate special procedures intended to root out any unknown infectees, as well as reduce or stop the pathogen’s spread to new patients.

Luckily, this strategy proved effective in all the reported cases.

“CDC’s study found several dangerous pathogens, hiding in plain sight, that can cause infections that are difficult or impossible to treat,” said CDC Principal Deputy Director Anne Schuchat, M.D. “It’s reassuring to see that state and local experts, using our containment strategy, identified and stopped these resistant bacteria before they had the opportunity to spread.”

The Vital Signs report explains that the CDC’s approach, when faced with such pathogens, calls for rapid identification of resistance, infection control assessments, testing patients who may carry and spread the germ (even those that don’t exhibit symptoms), coupled with continued infection control assessments until spread is stopped. Initial screening is performed within 48 hours of the initial report, and maintain follow-up procedures over several weeks to ensure the threat is neutralized.

CDC prevention strategy.

Image credits CDC.

The CDC estimates that such efforts prevented over one and a half thousand new cases of difficult-to-treat or potentially untreatable infections, including high-priority threats such as Candida auris and carbapenem-resistant Enterobacteriaceae (CRE). The AR Lab Network is crucial for this effort, as it allows for a coordinated response from several healthcare facilities, labs, health departments, and members of the CDC itself.

Other highlights published in the report include:

  • One in four germ samples sent to the AR Lab Network for testing had genetic mechanisms that allow them to spread resistance to other populations.
  • Investigations in facilities that work with unusual resistance pathogens show that about 10% of screening tests on patients without symptoms identified a hard-to-treat strain that spreads easily. This would suggest that germs can spread relatively undetected in such facilities.
  • For CRE alone, estimates show that the containment strategies would prevent as many as 1,600 new infections in three years’ time, in a single state — representing a 76% slash in the total number of cases.


So what can you do to help the CDC contain such dangerous pathogens in the future? Well, it’s not that much — as you can imagine, tackling populations of drug-resistant bacteria isn’t something you do for fun on a Wednesday evening if you want to be effective. But you can help by being the Center’s scout; its eyes on the ground, if you will. If you want to pitch in, the CDC recommends you:

  • Inform your health care provider if you recently received health care in another country or facility. This lets them tie the dots together and trace down a pathogen’s potential movements in case a threat is determined.
  • Talk to your healthcare provider about preventing infections, taking good care of chronic conditions and getting recommended vaccines. An ounce of prevention beats a pound of cure, as the old saying goes — especially if that pound of cure can’t even kill off the infection.
  • Lastly, practice good hygiene — such as keeping hands clean with handwashing or alcohol-based hand rubs — and make sure you keep cuts and other open wounds clean until healed.

The entire Vital Signs report, as well as more information on the CDC’s containment strategy,  can be accessed on the CDC’s website, here.

Left: Electron microscope image of a normal E. coli cell. Righl: an engineered cell with a mixed membrane, which shows an elongated form. Credit: University of Wageningen / Van der Oost laboratory.

Scientists engineer new life form with mixed Bacteria and Archaea membrane

Left: Electron microscope image of a normal E. coli cell. Righl: an engineered cell with a mixed membrane, which shows an elongated form. Credit: University of Wageningen / Van der Oost laboratory.

Left: Electron microscope image of a normal E. coli cell. Righl: an engineered cell with a mixed membrane, which shows an elongated form. Credit: University of Wageningen / Van der Oost laboratory.

The tree of life consists of three domains: Archaea, Bacteria, and Eukarya. The first two are all prokaryotic microorganisms, or single-celled organisms whose cells have no nucleus. Eukarya can be both unicellular and multicellular organisms. But what did the very first life forms look like? Scientists suspect that Bacteria and Archaea evolved from a hypothetical Last Universal Common Ancestor, or LUCA for short, because the organism’s cell membrane was an unstable mixture of lipids.

Dutch researchers at the University of Groningen engineered an E. coli bacterium whose membrane is both a mix of Bacteria and Archaea. They found that this mixed membrane was stable, refuting the main hypothesis for the ‘lipid divide.”

A mixed membrane new life form

Prof. Arnold Driessen. Credit: University of Groningen.

Prof. Arnold Driessen. Credit: University of Groningen.

A bacteria’s membrane is composed of straight-chain fatty acids that are ester-linked to a backbone of glycerol-3-phosphate. In Archaea, the backbone is glycerol-1-phosphate, to which isoprenoids are linked by ether bonds. According to the ‘lipid divide’ hypothesis, a mixed membrane of phospholipids would be less stable than a homogeneous membrane of just one type of phospholipid. “So eventually a split occurred, resulting in the two domains of Bacteria and Archaea,” commented Arnold Driessen, who is a Professor of Molecular Microbiology at the University of Groningen.

This split — if it ever happened — must have occurred 3.5 billion years ago. Alas, this primeval event has not been recorded in the fossil record, which left Driessen and colleagues with only one viable option: reverse-engineer a microorganism with a mixed membrane.

The University of Groningen researchers were not the first to attempt this endeavor. However, the previous trials engineered bacteria with no more than 1% archaeal lipids. Using a novel approach, Driessen and colleagues made a huge leap by devising a viable cell comprised of a staggering 30% archaeal lipids.

“The main challenge was to get E. coli cells to synthesize significant amounts of ether lipids. In the work there were two key elements, introduction in addition to the enzymes of the ether lipid pathway, the by us recently identified archaeol synthase; and the genomic duplication of the E. coli MEP/DOXP+ pathway to stimulate isoprenoid biosynthesis which is normally is at a low level. When both were brought together this led to the biosynthesis of significant amounts of ether lipids in E. coli and this was the ‘Aha’ moment!” Driessen told ZME Science.

In the left panel: EM image of a normal dividing E. coli cell. Right panel: an engineered cell with high archaeal lipid production, showing lobular irregularities in the cell membrane. Credit: University of Wageningen / Van der Oost laboratory.

In the left panel: EM image of a normal dividing E. coli cell. Right panel: an engineered cell with high archaeal lipid production, showing lobular irregularities in the cell membrane. Credit: University of Wageningen / Van der Oost laboratory.

In the newly engineered E. coli,  the phosphatidylglycerols — the lipids which form the basic bilayer of the bacterial membrane — were replaced by their archaeal equivalent (archaetidylglycerol). Despite this transformation, the bacterium grew normally and was stable, which refutes the hypothesis that a mixed membrane is inherently unstable. The new life form also exhibited some differences from the unmodified E. coli, such as a more elongated cell.

Although it refutes the ‘lipid divide’ hypothesis, the research does offer some clues as to what may have driven a Bacteria/Archaea divide. For one, the archaeal enzymes that are crucial for archaeal membrane lipids are less specific in the reactions they catalyze than the bacterial counterparts. Driessen believes enzyme specificity could have one of the drivers of the divide.

In any case, it’s a challenging inquiry because the reverse-engineering process is far from perfect. For one, the researchers modified a modern E. coli bacteria — the product of countless generations that evolved over the course of 3.5 billion years. When I asked Driessen how far he thinks scientists are from modeling a primordial organism, he wasn’t very optimistic — “surely far away from the primordial form, as the primordial organism had a completely different protein make up,” he said.

“The thing we mimic, if you can say so, is a mixed heterochiral membrane, and our data shows that this can lead to a stable organism suggestion that the lipid divide was not driven by an intrinsic instability of such membranes. Of course, this was a test with a system that evolved into what it is now, thus with membrane proteins that are used to function in a homochiral membrane. Apparently, these membrane proteins function readily is such ‘primordial’ membranes,” Driessen continued.

Next, the researchers plan on engineering an E. coli bacterium which relies entirely on archaeal ether lipids.

“We would like to replace the entire phosphatidylethanolamine (PE) pool for archatidylethanolamine (AE), to make an E. coli which relies entirely on archaeal ether lipids. However, this is far from trivial. PE is a non-bilayer lipid, AE shows a much more complex phase behavior, so it may not compensate for the polymorphic behavior of PE which is a requirement for viable E. coli,” Driessen said.

“Synthetic biology may be able to construct presumed primordial life forms such that evolution can be recreated in the laboratory so that we can start to test/challenge evolution theories. It is a challenge for an experimental evolutionary molecular biologist, but need to step away from the theory and validate hypotheses experimentally.”

Scientific reference: Antonella Caforio, Melvin Siliakus, Marten Exterkate, Samta Jain, Varsha Jumde, Ruben Andringa, Servé Kengen, Adriaan Minnaard, Arnold Driessen, John van der Oost, Converting Escherichia coli into an ‘archaebacterium’ with a hybrid heterochiral membrane, Proceedings of the National Academy of Sciences, 2018.


Petri dish.

New method developed to stop bacteria from sharing antibiotic resistance genes

The molecular mechanisms underpinning the spread of drug resistance in bacteria populations have been identified — and a new class of molecules has been designed to fight it.

Petri dish.

Image credits via Pixnio.

The rise of multi-drug resistant bacteria is often — and to my mind, as well as the WHO’s — rightly held to be one of the biggest current threats to global health. A large part of what constitutes this threat is that bacteria can share resistance among themselves — like IT guys swapping USB sticks with new firewall software, bacteria can share genes encoding antibiotic resistance.

In a bid to nip this growing threat in the bud, researchers at the European Molecular Biology Laboratory (EMBL) have uncovered and then unraveled one of the major resistance-transfer mechanisms. They’ve also developed proof-of-concept molecules to carry out this bacterial sabotage.

Resisting the resistance

Over time, bacteria have developed a certain resistance level to most drugs we use today. The worst are arguably those that have developed resistance to multiple classes of antibiotics; examples range from MRSA (methicillin-resistant Staphylococcus aureus), VRE (vancomycin-resistant enterococcus), and ESBL (extended spectrum beta-lactamase) producing Enterobacteriaceae.

One of the major drivers of resistance spread throughout bacterial populations are transposons. Also called ‘jumping DNA’, they are bits of genetic code that can autonomously move throughout the genome. When this movement occurs between bacteria, it spreads antibiotic resistance genes among individuals. Very bad for us.

Under the leadership of Orsolya Barabas, one research team at the EMBL became the first to determine the structure of a crystal-like, protein-DNA structure which inserts these transposons in recipient bacteria. Dubbed the transposase protein, this molecule could hold the key to throwing the whole process into disarray.

Protein structure.

The unusual shape of the transposase protein (blue) forces the transposon DNA (grey) to unwind and open up.
Image credits Cell.

The protein has an unusual shape, which allows it to bind to DNA in an inactive state, keeping the transposon safe from potential chemical or physical damage until it’s delivered to its new host. Its shape also forces the transposon DNA to unwind, the team notes, allowing the protein to insert these genes into a wide array of locations within the genomes of many different bacteria.

“If you think of ropes or wires, they are usually bundled and wound-up to make them stronger. If you want to tear or cut one, it’s much easier if you unwind and loosen it first,” says EMBL group leader Orsolya Barabas, who led the work.

“It’s the same for DNA, and the transposon transfer mechanism takes advantage of this.”

Because the transposase protein first unwinds and separates the transposon’s strands, they can more readily be cut and pasted to a new site in the recipient genome. Again, very bad for us.

Luckily, Barabas’ team used the protein’s crystal structure to develop molecules that should block the transposons’ movement through two mechanisms. The first prevents the transposase protein from activating by blocking its architecture with a newly designed peptide, a short chain of amino acids — in other words, it wedges itself in the transposase so that it can’t unfurl and deliver the DNA cargo.

The second method ‘corrupts’ the genetic data. This molecule, a DNA-mimic, binds to the transposon and blocks the DNA strand replacement in the host; no replacement, no resistance transfer.

“As we believe these features are broadly present in these jumping DNA elements, but not in related cellular systems, they may be quite specific to transposons. This way, we can target only the bacteria we want, and not the many good bacteria in our bodies and the environment,” Barabas explains.

The molecules are still far from trials with living hosts. For now, Barabas and her colleagues will focus on better understanding the transfer mechanisms, as well as on developing and testing new strategies to block it.

The paper “Transposase-DNA Complex Structures Reveal Mechanisms for Conjugative Transposition of Antibiotic Resistance” has been published in the journal Cell.


Small populations of bacteria can elude antibiotics — here’s how we’re fixing that

Small populations of bacteria respond differently to antibiotics than larger ones, a new study reports — offering clues as to why it’s so hard to kill these bugs off.


Image via Pixabay.

A population of bacteria that sports 100 or fewer cells doesn’t play by the rules; at least, not as far as antibiotics are concerned. Larger populations tend to respond homogeneously throughout their members, but with small populations, even antibiotics are more of a hail mary, new research shows — sometimes they work, sometimes they don’t, and it seems to be completely down to chance.

Strength in (small) numbers

Which, understandably, is not an ideal state of affairs for us hairless bipeds. Especially because for decades, the prevailing wisdom held that reducing the number of bacteria down to a few hundred individuals would be enough for the immune system to come in and carry the day.

“More recently, it became clear that small populations of bacteria really matter in the course of an infection,” says lead author Minsu Kim.

“The infectious dose — the number of bacterial cells needed to initiate an infection — turned out to be a few or tens of cells for some species of bacteria and, for others, as low as one cell.”

The researchers wanted to understand why antibiotic treatments sometimes work, and sometimes fail. They’ve started with the usual culprits: variations in immune responses between people, or possible mutations of bacteria that make them more virulent in some cases. Kim, however, wasn’t impressed. She suspected that something else was at work here, and her suspicions only became stronger when researchers working with model organism C. elegans recorded unexpected treatment failures even for antibiotic-susceptible infections.

Focusing their research only on small populations of bacteria, the team discovered that their interaction with antibiotics is based on a different dynamic than that of large populations. The researchers observed that antibiotics induce fluctuations in the density of bacterial populations as they kill off individuals, which they expected; however, they also noted that when the population’s rate of growth overcame the rate at which the antibiotics killed individuals, clearance failed.

Armed with this knowledge, they created a low-dose cocktail of drugs to preempt this quirky dynamic. This mix contained a bactericide (a compound that kills bacteria) and bacteriostat (a substance that slows the growth of bacteria). Taken together, these were intended to limit the random fluctuation seen by the team, and thus make it more probable to keep the population’s overall death rate higher than the growth rate. They then took this cocktail to the lab to see how it works. First, they showed that it was effective on a small population of drug-susceptible E. coli. Then they applied it to a clinically-isolated strand of antibiotic resistant E. coli — again, the cocktail worked.

“We’ve shown that there may be nothing special about bacterial cells that aren’t killed by drug therapy — they survive by random chance,” said Kim. “This randomness is a double-edged sword. On the surface, it makes it more difficult to predict a treatment outcome. But we found a way to manipulate this inherent randomness in a way that clears a small population of bacteria with 100 percent probability.”

“By tuning the growth and death rate of bacteria cells, you can clear small populations of even antibiotic-resistant bacteria using low antibiotic concentrations.”

The team hopes that their model cocktail can help guide development of more refined antibiotic treatment courses. Their end goal is to help researchers develop treatments that use lower doses to kill an infection entirely, for as many different infections as possible.

“It’s important because if you treat a bacterial infection and fail to kill it entirely, that can contribute to antibiotic resistance,” says Kim.

Not all antibiotics available today fit the model they’ve developed, however. More research is needed get this approach ready for use in a clinical setting.

Antibiotic resistance is a huge and growing problem. Essentially, it means that at some point in the future our drugs won’t be able to reliably protect against bacteria — or they could become useless against them altogether. Antibiotic resistance could lead to 10 million people dying each year by 2050, a total health care burden of $100 trillion, and a reduction of 2% to 3.5% in world Gross Domestic Product (GDP) by the same year.

The paper “Antibiotic-induced population fluctuations and stochastic clearance of bacteria” has been published in the journal eLife.


Copper-coated uniforms for medical staff could help shred bacteria in hospitals

Healthcare professionals might soon be bringing on the bling in the workplace, as UK and Chinese researchers designed copper-covered uniforms to help fight bacteria.


Image via PxHere.

Materials scientists from the University of Manchester, working with counterparts from several universities in China, have created a ‘durable and washable, concrete-like’ material made from copper nanoparticles. They’ve also developed a method of bringing this composite to textiles such as cotton or polyester, a world first.

Coppering out

Bacterial infections are a major health issue in hospitals across the world. These tiny prokaryotes spread throughout healthcare facilities on surfaces and clothing, leading to losses both of life and of funds. The issue becomes worse still after you factor in the rise of drug resistance in most strains, which is rendering our once-almighty antibiotics more and more powerless. So we need to look for alternative ways of dealing with them, ones that do not rely on antibiotics.

One increasingly promising set of tools in our fight against disease are precious metals, such as gold and silver, which have excellent antibacterial and antimicrobial properties. However, deploying these on the surfaces and clothing mentioned earlier runs into some pretty obvious problems: first, gold and silver are really expensive — after all, they literally used to be money. Secondly, they don’t lend that well to making practical clothes, especially in a hospital setting.

Enter copper. Less expensive than gold or silver, copper is nevertheless still very good at killing pathogens, which solves problem one. However, up to now, we still didn’t have an adequate answer to issue number two — which is what the team addresses in this paper.

Using a process dubbed ‘Polymer Surface Grafting’, the researchers were successful in tying copper nanoparticles to cotton or polyester using a polymer brush. Cotton and polyester were chosen as a test bed as they’re the most widely used natural fiber and a typical man-made synthetic fabric, respectively.

The materials were brushed over with copper nanoparticles measuring between 1 and 100 nm, which is really small — one nm equals one-millionth of a mm. The metal particles formed a strong, stable chemical bond with the cloth, meaning the metal won’t flake off or be washed away.

“Now that our composite materials present excellent antibacterial properties and durability, it has huge potential for modern medical and healthcare applications,” says lead author Dr Xuqing Liu, from UoM’s School of Materials.

During lab tests, the copper-coated materials easily killed Staphylococcus aureus (S. aureus) and E. coli, two of the most common and infectious bacteria in hospitals, even after being washed 30 times.

The team says their results are very promising, and Dr. Liu adds that “some companies are already showing interest” in developing it further.

“We hope we can commercialise the advanced technology within a couple of years,” he adds. “We have now started to work on reducing cost and making the process even simpler.”

The paper “Durable and Washable Antibacterial Copper Nanoparticles Bridged by Surface Grafting Polymer Brushes on Cotton and Polymeric Materials” has been published in the Journal of Nanomaterials.

Scientists find promising new antibiotic — in the soil

A team of researchers from Rockefeller University has discovered a new class of antibiotics — and they found it in soil bacteria.

Image in public domain.


In 1928, a rather absent-minded scientist called Alexander Fleming returned from a summer vacation in Scotland to find a messy workbench — and a good deal more. Dr. Fleming found that a mold called Penicillium notatum had contaminated his Petri dishes, which were filled with colonies of Staphylococcus aureus. He noted that where the mold had taken over, it prevented the normal growth of the staphylococci. This paved the way for the discovery of Penicillin, the world’s first synthetic antibiotic.

Antibiotics changed the world and ushered in a new age of medicine, opening the door for the treatment and prevention of numerous bacterial infections. But recently, antibiotics have been struggling to keep up. Antibiotic resistance is peaking around the world, and it’s becoming a massive threat — one which, according to the World Health Organization, we’re not prepared to deal with yet. There are several things we, as a society, need to do to tackle this problem, but one method — the brute force approach — is to discover new antibiotics to which pathogens haven’t adapted to yet.

In this aspect, microbiologist Sean Brady thinks it’s time to switch tactics. Instead of growing new antibiotics in the lab, he wants to find them out in the field — in this case, quite literally.

Brady and his colleagues extracted over a thousand soil samples from U.S. soils, sequencing bacterial DNA and looking for potential antibiotics. They struck gold.

“Every place you step, there’s 10,000 bacteria, most of which we’ve never seen,” said Brady, an associate professor at Rockefeller University in New York. “Our idea is, there’s this reservoir of antibiotics out in the environment we haven’t accessed yet,” he added.

In a study referenced below, he and his colleagues describe the discovery of a set of genes that produce malacidins, a new family of antibiotics. Malacidins are a class of antibiotics found in soil microbiomes but not reported in microbiological culture-based studies. Malacidins work in a different way than most antibiotics: they use calcium to disrupt bacterial cell walls, a mechanism to which microorganisms don’t seem to develop resistance.

To test how these antibiotics work, they tested samples on rats with induced MRSA skin infections, reporting that the new antibiotics successfully defeated the dreaded MRSA. Scientists don’t really know what cells produce the antibiotic, but then again, they don’t need to — they have something just as good: the genetic blueprint for building it. The only problem now, Brady says, is to scale it.

Of course, we won’t see this antibiotic on the shelves tomorrow. More trials are still required to better assess the efficacy and safety of the treatment for humans.

Journal Reference: Bradley M. Hover et al. Culture-independent discovery of the malacidins as calcium-dependent antibiotics with activity against multidrug-resistant Gram-positive pathogens.

The Search for Alien Life: We Have Been Looking in the Wrong Places

SETI Initiative. Source: Traces Online.

Humanity has pondered the existence of alien life for centuries. However, it has been in just the past 100 years or so that modern science has backed some of this thinking. Scientists of the late 1800’s and early 1900’s believed that objects appearing on the surface of Mars were canals constructed by aliens. Particularly, astronomer Percival Lowell believed this concept and promoted it in works such as the book Mars As the Abode of Life (1908).

This belief in the scientific community led to a huge amount of pop culture based around the concept of extraterrestrials. This has resulted in some people even believing in the existence of aliens like the ones in the movies. Who knows? They could be out there. But some wonder how probable their existence is.

With aliens constantly being depicted in entertainment, even after the Martian alien canal hypothesis was busted, scientists considered communicating with otherworldly life forms. The first scientists looking for a close encounter believed the best bet was to use radio waves as the communication medium. The first of such proposed experiments was conducted in 1960 by astronomer Frank Drake.

One of the most eye-opening quotes about extraterrestrial alien life comes from the book Time for the Stars by Alan Lightman. The author states, “Are we alone in the universe? Few questions are more profound… Extraterrestrial contact would forever change the way we view our place in the cosmos” (Lightman 21).

Drake would definitely not be the last scientist to attempt to summon a response from an alien. But this was the first modern example of tests which would now be referred to as part of SETI, the search for extraterrestrial intelligence. In 1980, to bring more of a public interest to SETI, the legendary astrophysicist, astronomer, and astrobiologist Carl Sagan and several others formed The Planetary Society. In more recent years, other programs with goals similar to SETI’s have been established such as METI, messaging extraterrestrial intelligence.

Apart from radio waves, humans have tried other ways of communicating with hypothetical aliens. One example is a plaque which was attached to the Pioneer 10 probe in 1972. This plaque would be a unique kind of “message in a bottle,” except the ocean it was doomed to drift in was far more vast than any sea on Earth. It was inquired of Carl Sagan about sending such a message several months before the scheduled departure of the craft. So Sagan went to work, and assisting him with this undertaking was none other than Frank Drake, the man who had conducted the first modern SETI tests in 1960. The fruit of numerous labors and laborers, the Pioneer 10 plaque that was sent into space depicted a man and a woman and several objects. Through the imagery, the scientists were trying to give any aliens who might see this plaque an idea of what humans are like and where Earth is located.

This could be the first big mistaken researchers are making. They are looking to make contact. They are putting their faith in a sci-fi movie concept. What these scientists are attempting to do is call up and have a conversation with an alien or, better yet, a race of aliens. This is not to say that SETI is pointless, but it might not be the most opportune method for seeking alien life.

Perhaps scientists should strive to discover life in its simpler forms. As Lee Billings of Scientific American states in a recent article, if you were able to travel to another planet it is likely “you would find a planet dominated by microbes rather than charismatic megafauna.” Many scientists are now suggesting microscopic organisms could be more plentiful throughout the cosmos than macroscopic creatures.

Microbes Are a Realistic Form of Alien Life. Source: Joi Ito’s PubPub.

A specific search for such minuscule life forms is not a new practice. Bacteria are, of course, microbes. Astrobiologists like Richard Hoover and Dave McKay have examined certain meteorites. Some of the microscopic structures found embedded in or on the space relics resemble bacteria. They have released their findings in past years. They have admitted that even though the fossilized structures appear to be remnants of bacteria there is still some skepticism as to whether those structures are alien in origin. This is because bacteria from Earth could have been attached to the meteorites once they entered our atmosphere.

So how do scientists narrow down the search for alien life even further? Billings’ piece may give us the best idea available at the moment. He informs his readers that one of oxygen’s properties is that it tends to descend from an atmosphere in the form of mineral oxides. It does not remain in its gaseous phase for long. Because of its nature, in an atmosphere such as Earth’s, the oxygen has to be reinstituted on a regular basis.

Astrobiologists have to accept oxygen may be one of the least familiar elements they come upon when studying potential life-supporting bodies. For example, atmospheric chemist David Catling has said the atmosphere of a world dominated by microscopic life could be largely comprised of methane and carbon dioxide gases. Keeping this in mind, this will hopefully narrow down the most likely planet candidates for life.

Gold nugget.

Research into nugget-forming bacteria paves the way to better gold extraction methods

An international team of researchers has uncovered the reactionary processes biology uses to bind gold. The process, which is employed by heavy-metal-resistant bacteria, could revolutionize how we extract the precious metal.

Gold nugget artsy.

Image credits Csaba Nagy.

Most organisms don’t really like high concentrations of heavy metals such as copper or gold, as they are quite toxic and pose a significant threat. However, certain beings, such as the bacterium C. metallidurans, have adapted to withstand very high concentrations with ease. It does this by extracting useful elements from compounds laden with heavy metals and then depositing the toxic bits.

One interesting (and potentially quite lucrative) side-effect of this process is that C. metallidurans excretes pure gold, which coalesces into nuggets. Knowing how fond humans are of shiny things, a team of researchers from the Martin Luther University in Halle-Wittenberg (MLU), the Technical University of Munich (TUM), and the University of Adelaide in Australia have identified the molecular processes that underpin this nuggeting.

The bug with the golden eggs

C. metallidurans is a rod-shaped bacterium that primarily colonizes soils enriched/polluted with numerous heavy metal compounds. While that sounds like the bacterium is a poor judge of real-estate, its choice in soil actually comes with significant perks. Chief among them is that other bacteria don’t want anything to do with this harsh environment. The second is that if you look past the “deadly toxic” aspect, heavy metal compounds are a surprisingly hearty source of energy.

“Apart from the toxic heavy metals, living conditions in these soils are not bad,” explains Professor Dietrich H. Nies, a microbiologist at MLU. “There is enough hydrogen to conserve energy and nearly no competition. If an organism chooses to survive here, it has to find a way to protect itself from these toxic substances.”

It was actually Nies himself, together with co-author Frank Reith, a Professor at the University of Adelaide, who found that C. metallidurans can deposit gold biologically back in 2009. However, they were unable to say why or how it did so — something they addressed in their new paper.

The process actually starts with copper. Copper is a vital trace element for C. metallidurans, however, the form it’s usually found geologically can’t be easily absorbed and processed by the bacteria. So the bacteria unleashes a barrage of chemical processes meant to soften up this copper and convert it to a form that’s easily gobbled up.

Gold enters the bacteria using the same processes and membrane channels as copper, the team reports. These compounds, by and large, resemble the copper ones, and so are processed by the same chemicals the bacterium uses for copper. Also, just like copper, gold becomes very toxic very fast at higher concentrations. The only difference is that C. metallidurans don’t actually want or need gold.

To make sure there isn’t too much of a copper buildup inside its membrane, the bacteria use an enzyme called CupA to pump any excess out, the team reports. However, when both metals are present in the cell, the CupA enzyme becomes suppressed, Nies explains. This poses quite a problem for the bacteria as the two metals “combined are actually more toxic than when they appear on their own.”

To flush out this extra-toxic cocktail, C. metallidurans employs a second enzyme dubbed CopA. This transforms both metals back into their original, hard-to-absorb forms.

“This assures that fewer copper and gold compounds enter the cellular interior,” Nies explains. “The bacterium is poisoned less and the enzyme that pumps out the copper can dispose of the excess copper unimpeded.”

“Another consequence: the gold compounds that are difficult to absorb transform in the outer area of the cell into harmless gold nuggets only a few nanometres in size.”


Gold nugget.

Gold nugget deposited by the bacteria.
Image credits L. Bütof et al., 2018, Metallomics.

The whole process takes toxic gold particles formed by erosion or other weathering processes and turns them into harmless gold nuggets. These nuggets are considered to be secondary gold, so called because they’re generated from primary (geologically-created) gold, broken down from ores and re-deposited.

The research completes our understanding of the biogeochemical gold cycle — the second half of which was largely unknown up to now. This cycle sees a bacterial transformation of primary gold metal into toxic compounds, followed by another, bacteria-powered transformation into secondary metallic gold in the last half of the cycle.

Fully understanding the processes involved in this cycle could help revolutionize the way we extract gold, making the process cleaner and more efficient. The most significant advantages over today’s methods would be the possibility to use poorer ores (with a small percentage of gold) than before and taking mercury and other very toxic compounds out of the extraction process.

The paper “Synergistic gold–copper detoxification at the core of gold biomineralisation in Cupriavidus metallidurans” has been published in the journal Metallomics.

E. coli with gas vesicles.

Scientists engineer air-filled bacteria they can track wiggling inside you with sound

One team of researchers trying to peer into the body took inspiration from submarine flicks and created a novel E. coli strain whose gas-filled protein sacks have the ability to reflect sound waves. They plan to use the bacteria to determine if treatments are making it to the desired spots in the body and working properly.

E. coli with gas vesicles.

Transmission electron micrograph (TEM) of an E. coli Nissle 1917 his bacterial cell engineered to contain gas vesicles (the lighter-colored structures inside). The cell is aprox. 2 micrometers in length.
Image credits Anupama Lakshmanan / Caltech.

Sometimes in medicine, we humans are frustratingly big compared to what we’re trying to heal. That makes is really hard to snoop around and see if the medicine we’re using gets to the right place and doing its job. It also doesn’t help that we’re quite opaque.

Hear here

One team of researchers is trying to work around both of those issues by making bacteria do the ‘seeing’ for us — using sonar. Their genetically-engineered strand of E. coli carries gas vesicles which can reflect incoming sound waves, in a process similar to how submarines reflect signals from sonar. The end goal is to inject such bacteria into a patient’s body to help fight disease — by targeting tumors, for example — and then using ultrasounds to determine their location. Such a technique would allow doctors to tell if treatments are making it to the right place in the body and whether or not they’re working as intended.

It’s not the first time anyone has considered using bacteria to fight illness. These little bits of life have shown great efficiency when treating disorders such as irritable bowel disease, and there is evidence suggesting they can be drafted to destroy cancer cells. However, the paper is the first to describe a reliable way of monitoring and drawing useful information from the bacteria while they’re deployed.

“We want to be able to ask the bacteria, ‘Where are you and how are you doing?'” says corresponding author Mikhail Shapiro.

“The first step is to learn to visualize and locate the cells, and the next step is to communicate with them.”

Similar approaches in the past have relied on light, mainly by ‘tagging’ cells with a “reporter gene” that encodes a fluorescent protein. However, such strategies have the decided disadvantage of only being usable in tissue samples removed from the body — because light can’t pass very deep through tissues.

Light through finger.

A bright light will pass through thin-ish tissue, however, and the results are quite cool.
Image credits New Savanna.

Shapiro’s team worked around this issue by substituting light for ultrasounds. Sounds — mechanical vibration — can pass through the body with relative grace compared to light. But that also poses an issue: sound can just as easily pass through bacteria.

Insulated prokaryotes

Shapiro says he had an epiphany six years ago, when he first learned about water-dwelling bacteria that regulate their buoyancy using gas-sacks (vesicles). These structures, he realized, could be used to bounce back sound waves enough to make the bacteria distinguishable from other types of cells (since gas is a much poorer carrier of sound than the surrounding tissues). The team proved that Shapiro’s approach works with ultrasounds — the things doctors use to look at babies in the womb — at least in the guts of mice.

Next, they had to move the genes encoding these vesicles from the original bacteria into something they could use medicinally. Their pick was Escherichia coli, which is commonly used in microbial therapeutics such as probiotics.

“We wanted to teach the E. coli bacteria to make the gas vesicles themselves,” says Shapiro. “I’ve been wanting to do this ever since we realized the potential of gas vesicles, but we hit some roadblocks along the way. When we finally got the system to work, we were ecstatic.”

Transferring the genetic blueprints into E. coli proved trickier than expected. The team first tried copy-pasting the genes isolated from a water-dwelling bacterium called Anabaena flos-aquae, but this failed to produce any gas-vesicles in the receiving bacteria. So they switched tactics and grafted the genes from Bacillus megaterium, a bacterium more closely related to E. coli. That didn’t work either.

Finally, the team mixed genes from both species, and this time it worked. The authors explain that the genes which encode the gas vesicles act like either bricks or cranes for the structures. Some of the proteins they encode are the actual building blocks, while others just help to glue everything together.

“Essentially, we figured out that we need the bricks from Anabaena flos-aquae and the cranes from Bacillus megaterium in order for the E. coli to be able to make gas vesicles,” says first author Raymond Bourdeau.

Further lab tests with mice showed that the engineered strain of E. coli could also be picked up using ultrasounds. The addition of the gas-vesicles doesn’t affect the bacteria’s viability. Being the “first acoustic reporter gene for use in ultrasound imaging,” it will still take a few years for the technology to be vetted enough for use in humans. However, the team is confident that it will “soon” be available for scientists who work with animals.

“We hope it will ultimately do for ultrasound what green fluorescent protein has done for light-based imaging techniques,” says Shapiro, “which is to really revolutionize the imaging of cells in ways there were not possible before.”

The paper “Acoustic reporter genes for noninvasive imaging of microbes in mammalian hosts,” has been published in the journal Nature.

Living Tattoo.

3D-printed “living tattoo” turns bacteria into sensors and computers you can wear

MIT researchers have developed “living” tattoos. They rely on a novel 3D printing technique based on ink made from genetically-programed cells.

Living Tattoo.

Image credits Xinyue Liu et al., 2017, Advanced Materials.

There seems to be a growing interest in living, 3D-printable inks these days. Just a few days ago, we’ve seen how scientists in Zurich plan to use them to create microfactories that can scrub, produce, and sense different chemical compounds. Now, MIT researchers led by Xuanhe Zhao and Timothy Lu, two professors at the institute, are taking that concept, and putting it in your skin.

The technique is based on cells programmed to respond to a wide range of stimuli. After mixing in some hydrogel to keep everything together and nutrients to keep all the inhabitants happy and fed, the inks can be printed, layer by layer, to form interactive 3D devices.

The team demonstrated their efficacy by printing a “living” tattoo, a thin transparent patch of live bacteria in the shape of a tree. Each branch is designed to respond to a different chemical or molecular input. Applying such compounds to areas of the skin causes the ‘tree’ to light up in response. The team says the technique can be sued to manufacture active materials for wearable tech, such as sensors or interactive displays. Different cell patterns can be used to make these devices responsive to environmental changes, from chemicals, pollutants, or pH shifts to more common-day concerns such as temperature.

The researchers also developed a model to predict the interactions between different cells in any structure under a wide range of conditions. Future work with the printing technique can draw on this model to tailor the responsive living materials to various needs.

Why bacteria?

Previous attempts to 3D print genetically-engineered cells that can respond to certain stimuli have had little success, says co-author Hyunwoo Yuk.

“It turns out those cells were dying during the printing process, because mammalian cells are basically lipid bilayer balloons,” he explains. “They are too weak, and they easily rupture.”

So they went with bacteria and their hardier cellular wall structure. Bacteria don’t usually clump together into organisms, so they have very beefy walls (compared to the cells in our body, for example) meant to protect them in harsh conditions. They come in very handy when the ink is forced through the printer’s nozzle. Again, unlike mammalian cells, bacteria are compatible with most hydrogels — mixes of water and some polymer. The team found that a hydrogel based on pluronic acid was the best home for their bacteria while keeping an ideal consistency for 3D printing.

“This hydrogel has ideal flow characteristics for printing through a nozzle,” Zhao says. “It’s like squeezing out toothpaste. You need [the ink] to flow out of a nozzle like toothpaste, and it can maintain its shape after it’s printed.”

“We found this new ink formula works very well and can print at a high resolution of about 30 micrometers per feature. That means each line we print contains only a few cells. We can also print relatively large-scale structures, measuring several centimeters.”

Gettin’ inked

The team printed the ink using a custom 3D printer they built — its based largely on standard elements and a few fixtures the team machined themselves.

A pattern of hydrogel mixed with cells was printed in the shape of a tree on an elastomer base. After printing, they cured the patch by exposing it to ultraviolet radiation. They then put the transparent elastomer layer onto a test subject’s hand after smearing several chemical samples on his skin. Over several hours, branches of the patch’s tree lit up when bacteria sensed their corresponding stimuli.

Logic gates with ink.

Logic gates created with the bacteria-laden ink. Such structure form the basis of computer hardware today.
Image credits Xinyue Liu et al., 2017, Advanced Materials.

The team also designed certain bacterial strains to work only in tandem with other elements. For instance, some cells will only light up when they receive a signal from another cell or group of cells. To test this system, scientists printed a thin sheet of hydrogel filaments with input (signal-producing) bacteria and chemicals, and overlaid that with another layer of filaments of output (signal-receiving) bacteria. The output filaments only lit up when they overlapped with the input layer and received a signal from them.

Yuk says in the future, their tech may form the basis for “living computers”, structures with multiple types of cells that communicate back and forth like transistors on a microchip. Even better, such computers should be perfectly wearable, Yuk believes.

Until then, they plan to create custom sensors in the form of flexible patches and stickers, aimed at detecting to a wide variety of chemical and biochemical compounds. MIT scientists also want to expand the living tattoo’s uses in a direction similar to that developed at ETH Zurich, manufacturing patches that can produce compounds such as glucose and releasing them in the bloodstream over time. And, “as long as the fabrication method and approach are viable” applications such as implants and ingestibles aren’t off the table either, the authors conclude.

The paper “3D Printing of Living Responsive Materials and Devices” has been published in the journal Advanced Materials.